La disrupción circadiana inducida por ftalato de di(2-etilhexilo) (DEHP) acelera los declives funcionales relacionados con el envejecimiento a través del estrés oxidativo y la señalización de insulina/IGF-1 en Caenorhabditis elegans

accumulation in aged animals. Antioxidant treatment with N-acetylcysteine partially alleviated these effects, supporting a key role for oxidative stress. Molecular docking and genetic analyses further demonstrated the involvement of insulin/IGF-1 signaling, with DEHP suppressing oxidative stress-induced nuclear translocation of DAF-16. Mutations in pathway genes attenuated DEHP-induced phenotypes. Collectively, these findings establish a mechanistic link between environmental phthalate exposure, circadian disruption, and aging-related functional declines mediated by oxidative stress and insulin/IGF-1 signaling.